scholarly journals Glutathione synthesis primes monocytes metabolic and epigenetic pathway for β-glucan-trained immunity

Redox Biology ◽  
2021 ◽  
Vol 48 ◽  
pp. 102206
Author(s):  
Haibo Su ◽  
Jiaxin Huang ◽  
Shufeng Weng ◽  
Baoying Zhang ◽  
Tianran Zhang ◽  
...  
2001 ◽  
Vol 120 (5) ◽  
pp. A502-A502
Author(s):  
T NODA ◽  
R IWAKIRI ◽  
K FUJIMOTO ◽  
T AW

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 130
Author(s):  
Munehiro Kitada ◽  
Yoshio Ogura ◽  
Itaru Monno ◽  
Jing Xu ◽  
Daisuke Koya

Enhanced oxidative stress is closely related to aging and impaired metabolic health and is influenced by diet-derived nutrients and energy. Recent studies have shown that methionine restriction (MetR) is related to longevity and metabolic health in organisms from yeast to rodents. The effect of MetR on lifespan extension and metabolic health is mediated partially through a reduction in oxidative stress. Methionine metabolism is involved in the supply of methyl donors such as S-adenosyl-methionine (SAM), glutathione synthesis and polyamine metabolism. SAM, a methionine metabolite, activates mechanistic target of rapamycin complex 1 and suppresses autophagy; therefore, MetR can induce autophagy. In the process of glutathione synthesis in methionine metabolism, hydrogen sulfide (H2S) is produced through cystathionine-β-synthase and cystathionine-γ-lyase; however, MetR can induce increased H2S production through this pathway. Similarly, MetR can increase the production of polyamines such as spermidine, which are involved in autophagy. In addition, MetR decreases oxidative stress by inhibiting reactive oxygen species production in mitochondria. Thus, MetR can attenuate oxidative stress through multiple mechanisms, consequently associating with lifespan extension and metabolic health. In this review, we summarize the current understanding of the effects of MetR on lifespan extension and metabolic health, focusing on the reduction in oxidative stress.


2020 ◽  
pp. 1-9
Author(s):  
Anaisa Valido Ferreira ◽  
Jorge Domiguéz-Andrés ◽  
Mihai Gheorghe Netea

Immunological memory is classically attributed to adaptive immune responses, but recent studies have shown that challenged innate immune cells can display long-term functional changes that increase nonspecific responsiveness to subsequent infections. This phenomenon, coined <i>trained immunity</i> or <i>innate immune memory</i>, is based on the epigenetic reprogramming and the rewiring of intracellular metabolic pathways. Here, we review the different metabolic pathways that are modulated in trained immunity. Glycolysis, oxidative phosphorylation, the tricarboxylic acid cycle, amino acid, and lipid metabolism are interplaying pathways that are crucial for the establishment of innate immune memory. Unraveling this metabolic wiring allows for a better understanding of innate immune contribution to health and disease. These insights may open avenues for the development of future therapies that aim to harness or dampen the power of the innate immune response.


2021 ◽  
pp. 104393
Author(s):  
Vera P. Mourits ◽  
Leonie S. Helder ◽  
Vasiliki Matzaraki ◽  
Valerie A.C.M. Koeken ◽  
Laszlo Groh ◽  
...  
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